Optogenetic activation of accessory olfactory bulb input to the forebrain differentially modulates investigation of opposite versus same-sex urinary chemosignals and stimulates mating in male mice

Surgical or genetic disruption of vomeronasal organ (VNO)-accessory olfactory bulb (AOB) function previously eliminated the ability of male mice to processes pheromones that elicit territorial behavior and aggression. By contrast, neither disruption significantly affected mating behaviors, although VNO lesions reduced males' investigation of nonvolatile female pheromones. We explored the contribution of VNO-AOB pheromonal processing to male courtship using optogenetic activation of AOB projections to the forebrain. Protocadherin-Cre male transgenic mice received bilateral AOB infections with channelrhodopsin2 (ChR2) viral vectors, and an optical fiber was implanted above the AOB. In olfactory choice tests, males preferred estrous female urine (EFU) over water; however, this preference was eliminated when diluted (5%) EFU was substituted for 100% EFU. Optogenetic AOB activation concurrent with nasal contact significantly augmented males' investigation compared to 5% EFU alone. Conversely, concurrent optogenetic AOB activation significantly reduced males' nasal investigation of diluted urine from gonadally intact males (5% IMU) compared to 5% IMU alone. These divergent effects of AOB optogenetic activation were lost when males were prevented from making direct nasal contact. Optogenetic AOB stimulation also failed to augment males' nasal investigation of deionized water or of food odors. Finally, during mating tests, optogenetic AOB stimulation delivered for 30 s when the male was in physical contact with an estrous female significantly facilitated the occurrence of penile intromission. Our results suggest that VNO-AOB signaling differentially modifies males' motivation to seek out female vs male urinary pheromones while augmenting males' sexual arousal leading to intromission and improved reproductive performance

Social status regulates kisspeptin receptor mRNA in the brain of Astatotilapia burtoni

The brain controls reproduction in response to relevant external and internal cues. Central to this process in vertebrates is gonadotropin-releasing hormone (GnRH1) produced in neurons of the hypothalamic-preoptic area (POA). GnRH1 released from the POA stimulates pituitary release of gonadotropins, which in males causes sperm production and concomitant steroid hormone release from the testes. Kisspeptin, a neuropeptide acting via the kisspeptin receptor (Kiss1r), increases GnRH1 release and is linked to development of the reproductive system in mammals and other vertebrates. In both fish and mammals, kiss1r mRNA levels increase in the brain around the time of puberty but the environmental and other stimuli regulating kisspeptin signaling to GnRH1 neurons remain unknown. To understand where kiss1r is expressed and how it is regulated in the brain of a cichlid fish, Astatotilapia burtoni, we measured expression of a kiss1r homolog mRNA by in situ hybridization and quantitative reverse transcription-PCR (qRT-PCR). We found kiss1r mRNA localized in the olfactory bulb, specific nuclei in the telencephalon, diencephalon, mesencephalon, and rhombencephalon, as well as in GnRH1 and GnRH3 neurons. Since males\u27 sexual physiology and behavior depend on social status in A. burtoni, we also tested how status influenced kiss1r mRNA levels. We found higher kiss1r mRNA levels in whole brains of high status territorial males and lower levels in low status non-territorial males. Our results are consistent with the hypothesis that Kiss1r regulates many functions in the brain, making it a strong candidate for mediating differences in reproductive physiology between territorial and non-territorial phenotypes. © 2010 Elsevier Inc

Behavioral and neuroendocrine correlates of displaced aggression in trout

In humans and other primates, violent actions performed by victims of aggression are often directed toward an individual or object that is not the original source of provocation. This psychological phenomenon is often referred to as displaced aggression. We demonstrate that displaced aggression is either rooted in evolutionarily conserved behavioral and neuroendocrine mechanisms, or represent a convergent pattern that has arisen independently in fish and mammals. Rainbow trout that briefly encountered large, aggressive fish reacted with increased aggression towards smaller individuals. There was a strong negative correlation between received aggression and behavioral change: Individuals subjected to intense aggression were subdued, while moderate assaults induced strong agitation. Patterns of forebrain serotonin turnover and plasma cortisol suggest that the presence of socially subordinate fish had an inhibitory effect on neuroendocrine stress responses. Thus, subordinate individuals may serve as stress reducing means of aggressive outlet, and displaced aggression towards such individuals appears to be a behavioral stress coping strategy in fishes

Prior stress and vasopressin promote corticotropin-releasing factor inhibition of serotonin release in the central nucleus of the amygdala

Corticotropin-releasing factor (CRF) is essential for coordinating endocrine and neural responses to stress, frequently facilitated by vasopressin (AVP). Previous work has linked CRF hypersecretion, binding site changes, and dysfunctional serotonergic transmission with anxiety and affective disorders, including clinical depression. Crucially, CRF can alter serotonergic activity. In the dorsal raphé nucleus and serotonin (5-HT) terminal regions, CRF effects can be stimulatory or inhibitory, depending on the dose, site, and receptor type activated. Prior stress alters CRF neurotransmission and CRF-mediated behaviors. Lateral, medial, and ventral subdivisions of the central nucleus of the amygdala (CeA) produce CRF and coordinate stress responsiveness. The purpose of these experiments was to determine the effect of intracerebroventricular (icv) administration of CRF and AVP on extracellular 5-HT as an index of 5-HT release in the CeA, using in vivo microdialysis in freely moving rats and high performance liquid chromatography (HPLC) analysis. We also examined the effect of prior stress (1 h restraint, 24 h prior) on CRF- and AVP-mediated release of 5-HT within the CeA. Our results show that icv CRF infusion in unstressed animals had no effect on 5-HT release in the CeA. Conversely, in rats with prior stress, CRF caused a profound dose-dependent decrease in 5-HT release within the CeA. This effect was long-lasting (240 min) and was mimicked by CRF plus AVP infusion without stress. Thus, prior stress and AVP functionally alter CRF-mediated neurotransmission and sensitize CRF-induced inhibition of 5-HT release, suggesting that this is a potential mechanism underlying stress-induced affective reactivity in humans